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NR507 Midterm Exam 2026/2027 | NR507 Advanced Pathophysiology Midterm Study Guide & Exam Prep | Chamberlain University NR 507 Practice Questions | Cellular Adaptation & Injury, Inflammation, Immunity, Hypersensitivity Reactions, Autoimmune Disorders, Gene

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Prepare for the NR507 Advanced Pathophysiology Midterm Exam 2026/2027 with a comprehensive study and practice resource designed for Chamberlain University graduate nursing students. NR-507 is an advanced pathophysiology course covering normal and abnormal human physiologic responses and the mechanisms underlying selected disease processes.

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NR507 Midterm Exam 2026/2027 | NR507 Advanced Pathophysiology
Midterm Study Guide & Exam Prep | Chamberlain University NR 507
Practice Questions | Cellular Adaptation & Injury, Inflammation,
Immunity, Hypersensitivity Reactions, Autoimmune Disorders,
Genetics, Neoplasia, Cancer Biology, Hematologic Disorders,
Cardiovascular Pathophysiology, Respiratory Disorders, Renal &
Urinary Disorders, Fluid & Electrolyte Imbalances, Acid-Base Balance,
Endocrine Disorders, Neurologic Disorders, Cellular Mechanisms,
Pathophysiologic Processes, Clinical Manifestations, Diagnostic
Findings & Advanced Nursing Clinical Judgment | Practice Questions &
Detailed Rationales
Question 1: Which cellular adaptation is characterized by a decrease in both cell
size and number, often resulting from decreased workload or diminished blood
supply?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
E. Dysplasia
CORRECT ANSWER: C. Atrophy
Rationale: Atrophy represents a reduction in cell size and number due to
decreased functional demand, denervation, ischemia, or nutrient deprivation.
Immobilization and chronic ischemia are classic clinical triggers. Hypertrophy
involves increased cell size, hyperplasia involves increased cell number,
metaplasia is replacement of one mature cell type by another, and dysplasia
denotes disordered growth.
Question 2: A client with long-standing hypertension develops an enlarged left
ventricle due to increased myocardial workload. This cellular adaptation is best
classified as:
A. Atrophy
B. Hypertrophy
C. Hyperplasia
D. Metaplasia
E. Anaplasia

,CORRECT ANSWER: B. Hypertrophy
Rationale: Hypertrophy is an increase in cell size, not number, in response to
increased functional demand or hormonal stimulation. The heart muscle enlarges
to compensate for chronic pressure overload. Hyperplasia involves cell
proliferation, which is uncommon in cardiac muscle.
Question 3: Which type of cellular adaptation involves an increase in the
number of cells in an organ or tissue in response to hormonal stimulation or
chronic irritation?
A. Atrophy
B. Hypertrophy
C. Hyperplasia
D. Metaplasia
E. Dysplasia
CORRECT ANSWER: C. Hyperplasia
Rationale: Hyperplasia is defined by an increase in cell number, often in tissues
capable of mitotic division. Physiologic examples include breast tissue during
pregnancy; pathologic examples include benign prostatic hyperplasia and
endometrial hyperplasia from unopposed estrogen. Hypertrophy is increased cell
size only.
Question 4: A chronic smoker undergoes biopsy of the bronchial epithelium,
which shows replacement of normal ciliated columnar cells with stratified
squamous cells. This finding is most consistent with:
A. Atrophy
B. Hypertrophy
C. Hyperplasia
D. Metaplasia
E. Neoplasia
CORRECT ANSWER: D. Metaplasia
Rationale: Metaplasia is a reversible change in which one adult cell type is
replaced by another cell type that is better able to survive adverse stimuli. In

,smokers, chronic irritation causes squamous metaplasia of the bronchial
epithelium. This is not malignancy but may predispose to dysplasia and neoplasia.
Question 5: Which cellular change represents disordered, non-neoplastic
proliferation characterized by variation in cell size, shape, and organization?
A. Atrophy
B. Metaplasia
C. Dysplasia
D. Anaplasia
E. Hypertrophy
CORRECT ANSWER: C. Dysplasia
Rationale: Dysplasia refers to abnormal cellular development with loss of
uniformity and architectural orientation. It is often a precancerous change but is
not invasive. Anaplasia denotes complete loss of differentiation seen in malignant
tumors.
Question 6: The most common cause of reversible cell injury in clinical practice
is:
A. Hypoxia
B. Free radical injury
C. Physical trauma
D. Viral infection
E. Nutritional deficiency
CORRECT ANSWER: A. Hypoxia
Rationale: Hypoxia (oxygen deprivation) is the most frequent and clinically
significant cause of cell injury. It leads to ATP depletion, failure of the sodium-
potassium pump, cellular swelling, and ultimately necrosis if prolonged. Free
radicals and infections are also injurious but less common as primary triggers.
Question 7: During hypoxic cell injury, the initial biochemical event that leads to
cellular swelling is:
A. Lysosomal rupture
B. ATP depletion and failure of the Na⁺/K⁺ ATPase pump

, C. Mitochondrial permeability transition
D. DNA fragmentation
E. Caspase activation
CORRECT ANSWER: B. ATP depletion and failure of the Na⁺/K⁺ ATPase pump
Rationale: Reduced oxidative phosphorylation decreases ATP production. Without
sufficient ATP, the sodium-potassium pump fails, causing sodium and water to
accumulate intracellularly, resulting in hydropic swelling. This is a reversible stage
if oxygen is restored promptly.
Question 8: Which type of cell death is characterized by cell shrinkage, nuclear
condensation, and absence of inflammation?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Apoptosis
D. Fat necrosis
E. Caseous necrosis
CORRECT ANSWER: C. Apoptosis
Rationale: Apoptosis is programmed cell death that occurs under physiologic and
pathologic conditions. It features cell shrinkage, chromatin condensation, and
formation of apoptotic bodies without invoking an inflammatory response.
Necrosis, by contrast, involves cell swelling, rupture, and inflammation.
Question 9: Coagulative necrosis is most commonly associated with ischemic
injury in which organ?
A. Brain
B. Heart
C. Pancreas
D. Lung
E. Liver
CORRECT ANSWER: B. Heart
Rationale: Coagulative necrosis preserves the basic tissue architecture with
hypereosinophilic cytoplasm and loss of nuclei. It is classically seen in ischemic

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